DIP Episode 107 - USMLE Step 1 Rapid Review Series 8 (GI)

Okay, welcome. My name is Divine. This is the 107th episode of the Divine Intervention Podcast and today I'll be continuing our USMLIS step one rapid review series. This will be series eight I believe and I will be discussing just clinical vignettes that are relevant to step one but today I'm gonna focus on GI so gastroenterology. So let's just jump right into it. So what if you get a question about a guy that has like you know pretty low argument and then they tell you that he has like an assarca like he has like a lot of like peripheral edema and they tell you that oh they perform an eGD of the stomach right so like an esophago gastrode-bued anoscopy that's the last time I'm gonna repeat that but an eGD of the stomach and they tell you that they see the rougue and the rougue of the stomach look huge. So what is that? That is Menetre's disease right? That's something also known as a protein-lucina interopathy. Okay now for a step one purposes right? If they give you a question about a patient that needs to be on an inset for like some serious medical condition but they have a peptic ulcer disease with that is there a particular reperture drug that you could use? You could use a misoprostol right? Remember misoprostol is a prostaglantin analogue so you're basically replacing the path of physiology because remember insides inhibitor cycloxyginase right? So that cuts down your synthesis of a prostaglantins right?

So by giving a prostaglantin analogue is essentially given what is missing right? Because remember prostaglantins are protective so they are protective for the GI tract right? So they sort of prevent acid secretion. Now what if you get a question about a guy you know that you know he has a history of like reflux and then he starts a medication and then he says doc over the last two months my breasts have gotten larger right? I really hope you think about like symedidine right? The H2 blockers remember those classically have a gynecomastia as a side effect okay? Now what if a person so let me give you two ulcer presentations? A lot of a person has like a history of ulcers and they tell you that when they eat the atomic hurts and these people are thin. What kind of ulcer are you thinking about? That's one of a gastric ulcer right? Because again if you have a gastric ulcer you're secreting it when you eat right? You gotta use acid to digest that food right? So as you're releasing that acid that will make whatever stomach ulcer hurts right? But what if you tell you that oh this person is tummy hurts but when you eat the tummy hurt goes away and this is a fat person right? That's a Diwali ulcer because I remember your Diwali ulcer has like burn or glance right? So you make bicarbon you eat to digest food so that will sort of like soothe the ulcer because bicarbon is basically like taking like those oral agents almost like taking like an antacid pretty much.

Now what's the antacid that has the big big big MBM association on diarrhea? That's magnesium hydroxide right? Okay now what if you get a question about like a 40-year-old lady over the last six months she's been having jaundice she's been itchy she has high levels of cholesterol what are you thinking about? So jaundice chronic problem itchy 40-year-old lady and let's assume she has a direct hyperbilarobinemia that is PVC right? So before it was called primary biliric cirrhosis but the name has changed it is now primary biliric colangitis remember the path of physiology kind of involves you having issues with your intra hepatic bowel dots okay contrast that with PSC where you have issues with your intra and extra hepatic bowel dots okay and remember that PVC is associated with antimidocontrolantibodies right? Okay now what if you get a question about a patient that has like elevated alkyphosph and they tell you that this patient is P-ancopositive right? I'm talking about PSC right? Remember PSC is one of those in fact I'll tell you this on your MBM is there are like three high-yield P-ancopathologies you want to know right? So primary sclerosis in colangitis is one and other one is microscopic polyangitis right?

and then the other one is you know synophilic granulomatosis with polyangitis or or trox trouts as syndrome those are like your high-yield P-ancopathologies the only C-ancopathology you really need to know about is Wagner's okay so maybe it's probably easier to remember that Wagner is a C-ancone they never know the thing is P-ancop okay now what is the classic I guess finding you'll see on imaging if a person has PSC right? Remember you see like that string of pearl sign on like ERCP for example or the me tell you like you see like this beads on the string pattern right? The beads beads on the string pattern and I mean if you even do like pathology you see like an onion skin appearance to the biliary system okay? Now what if a person they give you a question about a patient and they're AST 70 they're ALT 35 what are you thinking about? That is alcoholic hepatitis right?

Alcoholic hepatitis remember the scotch and tonic nummonic so AST to ALT is a 2 to 1 okay and actually this that will actually works pretty well clinically like I'll say I feel like 90% of the alcoholic patients have dealt with an intern year they have that AST to ALT where you should it's 2 to 1 okay and remember one high-yield lab in alcoholism is GGT so elevated GGT on an MBME you really really want to think about alcoholism under those circumstances okay and then what if you get a question about a patient that recently quit smoking and then they've started having like bloody there like over the last six months and they recently quit smoking that's another telltale sign of Australia if collided right? So smoking actually don't tell your patients to smoke obviously but smoking actually makes Australia if collided is better smoking makes Crohn's disease worse so you probably more put on an MBME but who knows you never know now what is the bug that could be asked let's assume you have an immigrant right and this immigrant has like a failure of his lower so the geosfinger to relax right so they show you like the birds big sign in like an immigrant is there a particular bug you want to think about you want to think about try try panosomac cruziar right?

Remember try panosomac cruziar causes big problems right causes like biggest of a glossy can cause ecalesia it causes big heart so you can cause a dilithic cardiomyopathy and then it also causes a big stomach right because you can cause herchprones disease right so you get herchprones so you have bacterial overgrown so your stomach distains with poop and stuff okay now if a person has alcoholic liver disease what's the term the pathologic term for the intracidoplasmic collections you see on histology right those are your malarie buddies right those are your malarie buddies okay now what if a person has like viral hepatitis what are those hipoptotic hepatocyte you can see on on histology we are called what?

Council man buddies okay what if you get a question about a patient this is like a 33 year old this 33 year old what has like a history of like liver problems and then you also have COPD that will be what alpha one antitrips in deficiency right remember it has a codominant inheritance okay now what if you do a colonoscopy and you see like a crap ton of polyps in like a 20 year old person what kind of gene mutation do they have right they have the FAP so they have familiar lathenomodos a polyposis right so like an APG APC tumor surface aging mutation remember that's a chromosome 5 for the purposes of the USML is another high-yoda chromosome 5 the solar you want to know is a kidney cuffman disease right that's what's also known as spinal muscular atrophy remember they have like it's otosomal recessive inheritance they have a mutation in like the survival moron neuron one gene on chromosome 5 okay otosomal recessive inheritance so that's like a kid it's it's pretty much always a kid less than a year old losing motor milestones having fast calculations if you see that that's a SMA spinal muscle atrophy remember you're killing the cells of the anterior horn okay now what if they give you a question and they tell you that they love histology with GI questions on the USML is just in case you've you've noticed from the way I'm focusing quite a bit on histology now what if they tell you that oh on histology you see like intrepithylial lymphocytes and this person has like my absorption in the Q-stem what are you thinking about or they may tell you that oh you see villas blunting what is that that's celiac disease right remember your anti endomisial and your anti tissue transglutamines are antibodies and remember that those people have a high risk of like a small bowel and a former if you don't avoid gluten or containing foods okay now what if a patient right they came into the

hospital they had a pneumonia you treated them with a course of antibiotics and then they have like pretty bad false million watery diarrhea what is that that's C-DeF right so that's so remember those colitis basically you should never get this wrong and then give me five you get this wrong after I take the exam go home and cry or something right because if you ever see a person gets antibiotics gets diarrhea afterwards there is nothing else that it is on mbm is it's C-DeF colitis it's super-membranos colitis okay now what if the give you a question about a patient that has like this just a super-specific scenario but if the terrier patient has like G-cell hyperplasia so like the G-cells the gastro-improducing cells of the of the stomach and they tell you that they have a mega-loblastic anemia what are you thinking about I hope you're thinking about this is one of those like 270 style questions on step one I don't if you guys remember a mag so autoimmune metaplastic excuse me atrophy gastritis they love to test that on the exams and they love to test it in the context of that like quarry because it's like if you've destroyed your parietal cells right then your G cells remember your G cell stimulator parietal cells so if your G cells are like where's my acid don't see any acid you try to make more gastric you want to get more gastric you want to increase the number of G of gastric producing cells so you get G-cell hyperplasia okay now what is the disease that's associated with a positive RNA and like anti-smut muscle antibodies that is what that's autoimmune hepatitis right that's a type one autoimmune hepatitis what are the antibodies that are found in type two autoimmune hepatitis those are your anti what liver kidney microsomal antibodies right so your anti LKM antibodies okay now what if a person has skip lesions in the GI tract on on imaging or on endoscopy what a

re you thinking about right that's Croose disease now there's this thing that we need to crop up on the USML is quite a bit don't forget that Croose disease has an association with antibodies against saccharomyces a cerevisia so like anti-ASCA antibodies that's something that's actually tested quite commonly on the USML definitely keep that in mind especially in more in more recent times okay now what if they give you a question about a child that has like painless like bloody poop and this is kind of been like a chronic problem and occasionally the child has like tenderness in the right lower quadrant and then let's say they tell you that you do like a nuclear scan like a nuclear medicine scan and you observe a lot of uptick in the right lower quadrant what are you thinking about I hope you're thinking about mechols diverticulum remember I can contain gastric neocoser so that can secret acid and then you can basically like bleed in your in your bowel and it's classically on MBM is in the right lower quadrant I remember that's mechols diverticulum it's a true diverticulum right what is I guess the false diverticulum that is associated like an old guy with bad breath so like the they won't put bad breath on an in-game you will put a halitosis to mess with your head what are you what are you going after there I hope you're thinking about zenkers diverticulum remember if you ask for your next best step in diagnosis you want to go ahead and perform like a barium swallow right remember they have like a weakness and like killions triangle around like the crackle fire angios muscle what else what else I want to say there yeah and it presents as bad breath and one thing you don't want to do on an MBM is to perform an EGD because there will be a high risk of perforation right be a high risk of perforation so they may give you a question about a person that has zenkers you do a

n EGD and then the patient becomes hypoxic and then they have like subcutaneous and physema you physically probably a suffigate so like call your general surgery friend send them to the OR if you don't send them to the OR quickly enough you have a dead patient right which is again not a good outcome so yeah don't never do an EGD if you suspect that zenkers are diverticulum okay now what if they tell you that a barium study reveals a bird big sun right what would that be that'll be what equalization right okay and if a person has right upper quadrant pain what is usually the first step on an MBM you want to get an ultrasound right a right upper quadrant ultrasound kind of the only like big exception to that rule is the patient has like the fever the right upper quadrant pain and the jaundice right and then let's see they're like super sick like hypotensive they have they have blood their temperatures like 103 right you're thinking about like a shackles triad right and like renal spent that remember renal spent that is the fever right upper quadrant pain jaundice and then they have like altered mental status and the hypotension that's a renal spent that that's a sending colon gyres your first step is to perform an ERCP okay and ERCP is both diagnostic and therapeutic for a sendin colon gyres okay now what did they give you a question about a patient you know they have a history of like they're like heavy drinkers and then they are complete of like abdominal pain and they get like a 25 out of 30 on like a mini mental status exam so they're kind of altered they have like some abdominal pain they have like low grade fever so let's say it's like the fever is like a hundred point nine what are you thinking about it really hope you're thinking about spontaneous bacterial periodtonitis okay for those people your next step in management is to get a percent thesis right and then

if you grab out more than if you look at the present thesis fluid you're like oh crap this person thesis fluid has more than 250 white cells that's all you need for your diagnosis of SBP you basically need to put those patients on something that cover equal life pretty much so like you can give like super fluxes in you can give I'll see probably super fluxes in mixed the most sense on an end being you can do like ampeicillin gentomisin and metronides all or I mean in the real world in the hospital you probably put those patients on zoosin but that's not what you don't an end be me because that is not good anti-biotic stewardship if you may okay now what if a person has hepatic and cephalopathy how do you treat that right you you can give lactolose right I will convert the lactolose convert the olactic acid or convert the ammonia to ammonia and then you peel it out or you poop it out and then you can also give this dropper foxyming or foxyming is an antibiotic it works pretty well for the treatment of it's kind of like Rayfampin refoxamine if I'm not mistaken it inhibits RNA polymerase so it's pretty good for the treatment of SBP I mean sorry of hepatic and cephalopathy okay now what are the drugs that you would want to potentially administer to a person that's having an acute varicil bleed so notice I'm very not my word in here I say acute varicil bleed you want to give them octriotide okay octriotide you can also use visopressin okay octriotide or visopressin now if a person has a history of varicis right and you want to profile acts against those varicis that is where things like a beta blocker like proprylonal and non-specific beta blocker like proprylonal and what's the name of this drug Spirinolactone that's where those things come in so beta blocker Spirinolactone you use them for chronic like prophylaxis in the acute phase of an esophageal varicil bleed octrio

tide is what is indicated under those circumstances okay now what did they give you a question about a guy you know he's had portal hypertension and then you've done some kind of procedure like an IR procedure to relieve that portal hypertension but a few days after this guy's like confused he's drowsy he's some no length he has like a coma what are you thinking about you're thinking about a tips procedure right that remember tips increases your risk of like worstening hepatic and cephalopathy okay and this is a beautiful beautiful beautiful anatomy question they can drop on an NVME exam right so if a person has like butchiaris syndrome or a person has cirrhosis what may preserve liver function in that patient like they can ask your name in question that oh this person will have hypertrophy of what of what part of the liver it's actually kind of high you to know that it's the cordic loop that will hypertrophy the reasoning behind that is remember the liver drains through the hepatic veins into the IVC that's not the case for the cordic loop the cordic loop actually drains directly into the IVC okay so hypertrophy of the cordic loop is a classic finding in a patient with cirrhosis or a patient with like butchiaris syndrome okay just one of those things you probably will never hear it anywhere but on this podcast I'll encourage you to keep that in your back pocket for the NVME exams I promise it's very high you to know that okay now what if they give you a question about like a 50 year old guy that has like heart problems and then they tell you that he also has my absorption and then they tell you that you do a small intestine like a small bowel biopsy and you see PES positive cells what are you thinking about that's we pose disease right that's a we pose disease remember it's from triferema we apply okay triferema we apply okay now what is the if a person has like has

like a set of menophaned toxicity on the liver what's the drug you can give you can give an acetylocysteine right okay now what if you get a question about a child a young kid let's assume it and this kid will be less than like six months old on an NVME they're never like more than a year old right six months old like a few weeks of life and let's say maybe this child got every through my scene for some weirdness or whatever and then the tell you that you have a poppable olive like mass right in the epic gastrum what are you thinking about that's by lyrics the no-sips right um classically if they ask for your next step in management so those kids will usually been been vomited or ton right so they'll have like they'll have like a metabolic alkalosis because they're puke you know that I said and remember the vomiting will be non-bilius right you'll be a non-bilius vomiting and then they'll also have like hypochylineal right because remember if you're vomiting you become volume down you become volume down you rev up the activity of your renein and your tensin out of the system so you become hypochylineal right remember your principal cell our dust will be doing its job so you'll be reabsorbing sodium and dumping potassium through that inek channel at the level and in through the so you're getting in the sodium through the inek channel and then you're dumping the potassium through the through the I believe they're called like rummage channels but you find them the collecting ducts principal cell area so you get hypochylineal so the thing is before you take those kids to surgery you need to fix all those electrolyte problems they have and hydrates them if not they'll die on the operating table right and you don't want that so as a clinical pro in general for person has significant electrolyte abnormalities they love to test this on like surgery shelf exams fix the electro

lyte problems first before you take them to surgery okay that's just really a smart thing to do so if a person has like significant uremia so like oh they are creatinies like seven the abu and it's like hundred right it's probably one of the pretty good to take them to surgery right there and there we want to go ahead and fix the electrolyte problems send them for dialysis or whatever before you then a procedure surgery okay now what if you get a question about a physician that is performing like a physical exam on a young child and this child has a long history of constipation and in this physician unfortunately gets like a projectile pups platter on his face what are you thinking about that is herch-prone's disease remember herch-prone disease a cerebral Down syndrome so it's like a neurocresscel remember Downs is basically explained by neurocresscel migration issues right think about all the Down syndrome problems like the herch-prones remember your neurocress cells make up your plexa that you find in your GI amicosa and then remember you're like your your endocardial cushions with you think they come from they come from neurocress as well right or your aortic opuminary septum where do you think that comes from come from neurocress can you sort of see how many of these Down syndrome problems appear to match up pretty nicely with issues relating to neurocresscel migration that is really the underlying pathophysiology behind many of the findings in Downs okay now what if a person is on chemotherapy or a patient is both stopped and they have like a lot of nausea a lot of vomiting what kind of drug can you give them you can give them on Down syndrome right on Down syndrome okay now what if they tell you that you perform a shillings test and you see vitamin B12 so the shillings test I've described it many times in many different podcasts that I have made but because the

se are happy to review I'm gonna move pretty quickly through this what if they tell you that you perform a shillings test and you find vitamin B12 in the urine after you've initially like basically saturated the entire bodies with B12 that's a no more result right but what if they tell you that you perform a shillings test you see B12 in the urine and let's see how do I put it so let me think of how weird this has a question let's see okay you know what let me just go ahead and describe the shillings test yeah it's just easier than framing you know take way too much thinking time to make a question but basically the shillings test is like if you were born like 300 years ago I don't know that's how you diagnose a B12 deficiency right so you're like oh this person has B12 deficiency okay great let me try to figure out what's causing it right because B12 deficiency it can come across by many things right you can get B12 deficiency from I don't know like pernicious anemia where you've used autoimmune like autoimmune attack of your pride ourselves or intrinsic factor or you can have like terminal helium problems like Crohn's disease right or like Celiac disease those things can all cause B12 issues right so basically the way you do the shillings test is you give the person like a very high IV dose of B12 so you saturate all the receptors right and then all the stores of B12 so let's assume you then give those people B12 early right and then you check the urine and you don't see the B12 you're like hey why might not see B12 in the urine if you're not seeing B12 in the urine it means that it could mean one of two things I mean there are many causes but it could be one of two things on an MDMA exam it could mean that oh maybe this person does not have maybe this person does not have intrinsic like has an intrinsic factor deficit basically or it could mean that your terminal h

elium is not working but now let's assume you administer excuse me you administer intrinsic factor and now you see B12 in the urine that tells you that the B12 deficiency was fixed by giving intrinsic factor so that means those people were potentially lacking intrinsic factor to appropriately reabsorbed the B12 across the terminal helium so if giving B if giving intrinsic factor fixes the problem use media diagnosis of prenexious anemia but if giving intrinsic factor does not help you still see the the B12 in the urine that tells you that they have more of like a reabsorption problem right so like the terminal helium is not so screwed up so they have like the B12 deficiency with that although another way they can try to mess with your head on MDM As with regards to this she links test is basically the person if a person has problems at the level of the terminal helium or any problem like with reabsorbing stuff in the GI tract they will have an abnormal desilose test desilose is just something that if your brushboarder is intact you can reabsorb it just fine but if you are not reabsorbing desilose that means your brushboarder is all screwed up somehow in some way shape or form so that's one weird principle I'll keep at the back of your mind if I were you are taking any of the USMLE exams okay so I think I'm gonna go ahead and stop here as I always say I do offer one or one to do it for the USMLE Step 1 2 CK 2 CSN Step 3 exams preclinical exams in med school 30-year-shelf exams the medicine board exams so the ABIM exam the medicine training exam and then if you're a med student applying to residency so an ERAS app or a college student applying to med school so an AMCA-SAP or if you need a like consulting for those things pretty much right so like interview prep personal statement writing prepare the application to give you the best foot forward I do offer like basically co

nsulting for those things I've done that with tons of people and pretty much everyone I've worked with has matched most of them to their first choices so if you need help with any of those things don't be afraid to reach out just send me an email through the website or to divine intervention podcasts podcasts with an S at the end at gmail.com and I'm usually pretty quick at responding and then if you also know a college student that is doing like organic chemistry general chemistry physics biochemistry physiology histology I do offer tutoring for most of pretty much all those states so I wish you all the best have a wonderful rest of your night and I really hope that the raptors win the MBA championship this year I just don't want go against the worst to win I have probably invited a few enemies by saying this but anyhow it's my podcast I can say whatever I want so I'll see you next time have a wonderful night and God bless you thank you

Proton pump inhibitors (PP Is) or H2 blockers, but specifically, misoprostol (a prostaglandin analogue) can replace the lost protective prostaglandins.

H2 blockers (e.g., cimetidine).

Duodenal ulcer.

Primary Sclerosing Cholangitis (PSC), Microscopic Polyangiitis, and Granulomatosis with polyangiitis (GPA).

"Beads-on-a-string" appearance.

Hypochloremic Metabolic Alkalosis (due to loss of gastric acid).

Clostridioides difficile (C. diff) infection, usually following antibiotic use.

Anti-mitochondrial antibodies (AMA).

Barium swallow; EGD (due to high risk of perforation).

Ratio $\ge 2:1$; Elevated GGT.

PBC involves small bile ducts and AMA; PSC involves larger intra- and extrahepatic bile ducts, often associated with pANCA.

Right lower quadrant; contains gastric mucosa (can secrete acid).

Clostridioides difficile (C. diff) infection, usually following antibiotic use.

Anti-mitochondrial antibodies (AMA).

Barium swallow; EGD (due to high risk of perforation).

Ratio $\ge 2:1$; Elevated GGT.

PBC involves small bile ducts and AMA; PSC involves larger intra- and extrahepatic bile ducts, often associated with pANCA.

Right lower quadrant; contains gastric mucosa (can secrete acid).